Gadolinium during human pregnancy following administration of gadolinium chelate before pregnancy.

Gadolinium (Gd), a toxic rare earth element, has been shown to dissociate from chelating agents and bioaccumulate within tissues, raising concerns about the possibility of their remobilization during pregnancy with subsequent free Gd exposures to developing fetuses. Gd chelates are among the most commonly used magnetic resonance imaging (MRI) contrast agents. This investigation was undertaken after the detection of elevated Gd (800-1000× higher than the usual rare earth element levels) in preliminary unpublished studies from the placentae of subjects in the NIH ECHO/UPSIDE Rochester Cohort Study and unpublished studies from placentae analyzed in formalin-fixed placental specimens from Surgical Pathology at the University of Rochester. Fifteen pregnancies with elevated Gd were studied (12 first pregnancies and 3 second pregnancies). Maternal bloods were collected from all three trimesters, maternal, and cord (fetal) bloods at delivery as well as placental tissue. Breastmilk was also collected from selected mothers. It was determined that Gd was present in maternal bloods from all three trimesters, and in cord bloods and breastmilk in both first and second pregnancies. These results emphasize the need to fully appreciate the implications of pre-pregnancy exposure to Gd chelates and its potential effects on maternal and fetal health.

A case of spontaneous basal ganglia hemorrhage with contralateral extension utilizing the canal of Gratiolet.

BACKGROUND: Intracranial hemorrhage accounts for 10-20% of stroke etiologies annually. Basal ganglia is the most common site for intracranial hemorrhage accounting for 50% of all cases. Bilateral spontaneous basal ganglia hemorrhages (BGH) are rare with few reported cases. CASE PRESENTATION: We report an unusual case of a 69-year-old female who presented with a spontaneous bilateral basal ganglia hemorrhage secondary to a right BGH with contralateral extension through the anterior commissure (AC) utilizing the Canal of Gratiolet. Clinical course and imaging findings are discussed. CONCLUSIONS: To our knowledge, this is the first case to specifically detail the extension of spontaneous hemorrhage across the AC via the Canal of Gratiolet, and imaging findings provide a novel depiction of AC anatomy and fiber distribution in a clinical context. These findings may explain the mechanism behind this rare clinical entity.

Role of non-classical monocytes in HIV-associated vascular cognitive impairment.

Despite antiretroviral treatment (cART), people living with HIV (PLWH) are more susceptible to neurocognitive impairment (NCI), probably due to synergistic/additive contribution of traditional cerebrovascular risk factors. Specifically, altered blood brain barrier (BBB) and transmigration of inflammatory monocytes are risk factors for developing cerebral small vessel disease (CSVD). In order to investigate if inflammatory monocytes exacerbate CSVD and cognitive impairment, 110 PLWH on cART and 110 age-, sex- and Reynold’s cardiovascular risk score-matched uninfected individuals were enrolled. Neuropsychological testing, brain magnetic resonance imaging and whole blood analyses to measure platelet-monocyte interaction and monocyte, endothelial activation were performed. Results demonstrated that PLWH exhibited increased levels of platelet-monocyte complexes (PMCs) and higher expression of activation molecules on PMCs. PLWH with CSVD had the poorest cognitive performance and the highest circulating levels of non-classical monocytes which exhibited significant inverse correlation with each other. Furthermore, markers of monocyte and endothelium activation were significantly positively correlated indicating BBB impairment. Our results confirm that interaction with platelets activates and drives monocytes towards an inflammatory phenotype in PLWH. In particular, elevated levels of non-classical monocytes may represent a common pathway to neuroinflammation, CSVD and subsequent cognitive impairment, warranting further longitudinal studies to evaluate responsiveness of this potential biomarker.

Brain lesions disrupting addiction map to a common human brain circuit.

Drug addiction is a public health crisis for which new treatments are urgently needed. In rare cases, regional brain damage can lead to addiction remission. These cases may be used to identify therapeutic targets for neuromodulation. We analyzed two cohorts of patients addicted to smoking at the time of focal brain damage (cohort 1 n = 67; cohort 2 n = 62). Lesion locations were mapped to a brain atlas and the brain network functionally connected to each lesion location was computed using human connectome data (n = 1,000). Associations with addiction remission were identified. Generalizability was assessed using an independent cohort of patients with focal brain damage and alcohol addiction risk scores (n = 186). Specificity was assessed through comparison to 37 other neuropsychological variables. Lesions disrupting smoking addiction occurred in many different brain locations but were characterized by a specific pattern of brain connectivity. This pattern involved positive connectivity to the dorsal cingulate, lateral prefrontal cortex, and insula and negative connectivity to the medial prefrontal and temporal cortex. This circuit was reproducible across independent lesion cohorts, associated with reduced alcohol addiction risk, and specific to addiction metrics. Hubs that best matched the connectivity profile for addiction remission were the paracingulate gyrus, left frontal operculum, and medial fronto-polar cortex. We conclude that brain lesions disrupting addiction map to a specific human brain circuit and that hubs in this circuit provide testable targets for therapeutic neuromodulation.

Increased risk for cerebral small vessel disease is associated with quantitative susceptibility mapping in HIV infected and uninfected individuals.

The aim of this study was to assess, in the context of cerebral small vessel disease (CSVD), whether cardiovascular risk factors and white matter hyperintensities (WMHs) were associated with brain tissue susceptibility as measured by quantitative susceptibility mapping (QSM). Given that CSVD is diagnosed by the presence of lacunar strokes, periventricular and deep WMHs, increased perivascular spaces, and microbleeds, we expected that QSM could capture changes in brain tissue due to underlying CSVD pathology. We compared a cohort of 101 HIV-infected individuals (mean age ± SD = 53.2 ± 10.9 years) with mild to moderate cardiovascular risk scores, as measured by the Reynolds risk score, to 102 age-matched controls (mean age (SD) = 50.3 (15.7) years) with similar Reynolds scores. We performed brain MRI to assess CSVD burden by acquiring 3D T1-MPRAGE, 3D FLAIR, 2D T2-TSE, and mGRE for QSM. We found that signs of CSVD are significantly higher in individuals with HIV-infection compared to controls and that WMH volumes are significantly correlated with age and cardiovascular risk scores. Regional QSM was associated with cardiovascular risk factors, age, sex, and WMH volumes but not HIV status. These results suggest that QSM may be an early imaging marker reflective of alterations in brain microcirculation.

The correlation of fractional anisotropy parameters with Ki-67 index, and the clinical implication in grading of non-enhancing gliomas and neuronal-glial tumors.

PURPOSE: To investigate the correlation between the FA parameters and Ki-67 labeling index, and their diagnostic performance in grading supratentorial non-enhancing gliomas and neuronal-glial tumors (GNGT). METHODS: This institutional review board-approved, Health Insurance Portability and Accountability (HIPAA) compliant retrospective study enrolled 35 patients, including 19 with low grade GNGT and 16 with high grade GNGT. The mean FA, maximal FA and mean maximal FA values derived from diffusion tensor imaging were measured. The correlation between the FA parameters and the Ki-67 labeling index was assessed by Spearman rank test. The receiver operating characteristic curve analysis and multivariate logistic regression analysis were performed to detect the optimal imaging parameters in grading GNGT. RESULTS: The three FA parameters of low grade GNGT were significantly lower than the high grade GNGT (p < 0.001). The mean FA, maximal FA and mean maximal FA had significant positive correlation with Ki-67 labeling index (p = 0.001, p < 0.001, p < 0.001 respectively). The maximal FA showed a higher sensitivity and specificity in grading of non-enhancing GNGT with specificity of 78.9%, sensitivity of 100.0%, respectively. CONCLUSIONS: The FA parameters correlated with Ki-67 labeling index, and were useful surrogates in preoperative grading supratentorial non-enhancing GNGT.

Pathomechanisms of HIV-Associated Cerebral Small Vessel Disease: A Comprehensive Clinical and Neuroimaging Protocol and Analysis Pipeline.

Rationale: We provide an in-depth description of a comprehensive clinical, immunological, and neuroimaging study that includes a full image processing pipeline. This approach, although implemented in HIV infected individuals, can be used in the general population to assess cerebrovascular health. Aims: In this longitudinal study, we seek to determine the effects of neuroinflammation due to HIV-1 infection on the pathomechanisms of cerebral small vessel disease (CSVD). The study focuses on the interaction of activated platelets, pro-inflammatory monocytes and endothelial cells and their impact on the neurovascular unit. The effects on the neurovascular unit are evaluated by a novel combination of imaging biomarkers. Sample Size: We will enroll 110 HIV-infected individuals on stable combination anti-retroviral therapy for at least three months and an equal number of age-matched controls. We anticipate a drop-out rate of 20%. Methods and Design: Subjects are followed for three years and evaluated by flow cytometric analysis of whole blood (to measure platelet activation, platelet monocyte complexes, and markers of monocyte activation), neuropsychological testing, and brain MRI at the baseline, 18- and 36-month time points. MRI imaging follows the recommended clinical small vessel imaging standards and adds several advanced sequences to obtain quantitative assessments of brain tissues including white matter microstructure, tissue susceptibility, and blood perfusion. Discussion: The study provides further understanding of the underlying mechanisms of CSVD in chronic inflammatory disorders such as HIV infection. The longitudinal study design and comprehensive approach allows the investigation of quantitative changes in imaging metrics and their impact on cognitive performance.

Advanced Neuroimaging in the Evaluation of Spinal Cord Tumors and Tumor Mimics: Diffusion Tensor and Perfusion-Weighted Imaging.

Spinal cord tumors are an important component of pathologic diseases involving the spinal cord. Conventional magnetic resonance (MR) imaging only provides anatomical information. MR diffusion tensor imaging (DTI) and MR perfusion-weighted imaging (PWI) may detect microstructure diffusion and hemodynamic changes in these tumors. We review recent application studies of MR DTI and PWI in spinal cord tumors. Overall, MR DTI and MR PWI are promising imaging tools that are especially useful in improving differential diagnosis between spinal cord tumors and tumor mimics, preoperative evaluation of resectability, and providing assistance in surgical navigation.

Immediate and Sustained Decrease in Smoking Urges After Acute Insular Cortex Damage.

INTRODUCTION: Smoking urges are fundamental aspects of nicotine dependence that contribute significantly to drug use and postquit relapse. Recent evidence has indicated that damage to the insular cortex disrupts smoking behaviors and claims to reduce urges associated with nicotine use, although tools that assess urge have yet to be used to validate these findings. We examined the effect of insular versus non-insular damage on urge using a well-accepted urge scale. METHODS: This 3-month observational prospective cohort study consisted of 156 current smokers hospitalized for acute ischemic stroke (38 with insular infarctions, 118 with non-insular infarctions). During hospitalization, the Questionnaire of Smoking Urges (QSU)-brief was assessed retrospectively based on experiences before the stroke (baseline, T0), prospectively immediately following the stroke (T1) and once more via telephone at 3-month follow-up (T2), with higher scores indicating greater urge. Bivariate statistics and multivariable linear regression were used to evaluate differences in QSU-brief scores, relative to baseline, between exposure groups, controlling for age, baseline dependence, stroke severity, use of nicotine replacement, and damage to other mesocorticolimbic regions. RESULTS: A greater reduction in QSU-brief score was seen in the insular group compared to the non-insular group from T0 to T1 (covariate-adjusted difference in means of -1.15, 95% CI: -1.85, -0.44) and similarly from T0 to T2 (covariate-adjusted difference in means of -0.93, 95% CI: -1.79, -0.07). CONCLUSIONS: These findings confirm the potential role of the insula in regulating nicotine-induced urges and support the growing evidence of its novelty as a key target for smoking cessation interventions. IMPLICATIONS: Human lesioning studies that evaluate the insula's involvement in maintaining nicotine addiction make inferences of the insula's role in decreasing urge, but do not use validated instruments that directly assess urges. This study corroborates prior findings using the continuous Questionnaire of Smoking Urges to quantify changes in urge from before lesion onset to immediate and 3-month follow-up time points.

Damage to the insula leads to decreased nicotine withdrawal during abstinence.

BACKGROUND AND AIMS: Current pharmacotherapies for tobacco dependence are generally well tolerated, but have relatively high rates of relapse. They target primarily the brains' mesocorticolimbic 'reward' pathway. However, recent evidence suggests that the insular cortex, a central cerebral hemispheric region historically overlooked in addiction models, may also play an important role in cognitive and emotional processes that facilitate drug use. We examined whether insular versus non-insular damage from ischemic stroke attenuated acute withdrawal from cigarette smoking and reduced the likelihood of nicotine replacement therapy (NRT) use during hospitalization. DESIGN: Data were derived from a longitudinal study with 3 months' follow-up, beginning June 2013 and ending May 2014. SETTING: Three acute care hospitals in Rochester, NY, USA. PARTICIPANTS: One-hundred and fifty-six current smokers hospitalized for acute ischemic stroke (38 with insular infarctions and 118 with non-insular infarctions, assessed by three neuroradiologists). MEASUREMENTS: The Wisconsin Smoking Withdrawal Scale (WSWS) and Minnesota Nicotine Withdrawal Scale (MNWS) were administered during hospitalization (a period of forced abstinence) to assess the frequency and severity of withdrawal symptoms. NRT use was also assessed during hospitalization. FINDINGS: On average, smokers with insular damage had a lower WSWS score during admission [mean=5.89, standard deviation (SD)=4.72] compared with those with non-insular damage (mean=9.20, SD=4.71; P<0.001) [covariate-adjusted difference in means of -3.12, 95% confidence interval (CI)=-4.97, -1.27]. A similar difference was also noted when the MNWS was used (P=0.02). Furthermore, participants with insular lesions appeared to be less likely to use NRT during admission compared with those with non-insular lesions [odds ratio (OR)=0.72, 95% CI=0.32, 1.64]. CONCLUSIONS: Current smokers with damage to their insular cortex brain region appear to experience fewer and less severe tobacco withdrawal symptoms, and appear to be less likely to require nicotine replacement therapy during hospitalization, compared with smokers with non-insular damage. These findings support the potential role of the insular cortex in regulating withdrawal during abstinence, a motivator responsible for the maintenance of addictive behaviors.

Smoking cessation behaviors three months following acute insular damage from stroke.

BACKGROUND: Recent evidence suggests that the insular cortex may play an important role in cognitive and emotional processes that facilitate drug use but it is unclear whether changes to the insula would result in sustained abstinence. To better understand the role of the insula in maintaining abstinence, we examined quitting patterns in smokers with acute damage to their insula relative to other regions. DESIGN: Prospective cohort study with 3month follow-up, beginning June 2013 and ending May 2014. SETTING: Three acute care hospitals in Rochester, NY. PARTICIPANTS: One-hundred-fifty-six current smokers hospitalized for acute ischemic stroke; 38 with insular infarctions and 118 with non-insular infarctions, assessed by 3 neuroradiologists. MEASUREMENTS: Self-reported smoking status (seven-day point prevalence and continuous abstinence), complete abstinence from any nicotine product, and disruption of smoking addiction (defined by criteria on smoking status, difficulty of quitting, and urge) were assessed at three months post-stroke. Time to relapse (in days) after discharge was also assessed. RESULTS: Insular damage was associated with increased odds of three-month continuous abstinence (OR=3.71, 95% CI: 1.59, 8.65) and complete cessation from any nicotine product (OR=2.72, 95% CI: 1.19, 6.22). Average time to relapse was longer in the insular-damaged group (17.50days, SD=19.82) relative to non-insular damage (10.42days, SD=18.49). Among quitters, insular damage was also associated with higher relative odds of experiencing a disruption of addiction compared to non-insular damage (adjusted OR=5.60, 95% CI: 1.52, 20.56). CONCLUSIONS: These findings support the potential role of the insular cortex in maintaining smoking and nicotine abstinence. Further research is needed to establish whether the insula may be a novel target for smoking cessation interventions.

64-detector CT angiography within 24 hours after carotid endarterectomy and correlation with postoperative stroke.

OBJECT: Carotid endarterectomy (CEA) carries a small but not insignificant risk of stroke/transient ischemic attack (TIA), most frequently observed within 24 hours of surgery, which can lead to the need for urgent vascular imaging in the immediate postoperative period. However, distinguishing expected versus pathological postoperative changes may not be straightforward on imaging studies of the carotid artery early after CEA. The authors aimed to describe routine versus pathological anatomical findings on CTA performed within 24 hours of CEA, and to evaluate associations between these CTA findings and postoperative stroke/TIA. METHODS: The authors reviewed 113 consecutive adult patients who underwent postoperative CTA within 24 hours of CEA at a single academic institution. Presence and location of arterial "flaps," luminal "step-off," intraluminal thrombus and hematoma were documented from postoperative CTA scans. Medical records were reviewed to determine the incidence of new postoperative neurological findings. RESULTS: Postoperative CTA findings included common carotid artery (CCA) step-off (63.7%), one or more intraarterial flaps (27.4%), hematoma at the surgical site (15.9%), and new intraluminal thrombus (7.1%). Flaps were seen in the external carotid artery (ECA), internal carotid artery (ICA), and CCA in 18.6%, 9.7%, and 6.2% of patients, respectively. New postoperative neurological findings were present in 7.1% of patients undergoing CTA. Flaps (especially ICA/CCA) and/or intraluminal thrombi were more frequently seen in patients undergoing CTA for new postoperative stroke/TIA (85.7%) versus patients undergoing CTA for routine postoperative imaging (14.3%, p = 0.002). CONCLUSIONS: CTA within 24 hours of CEA demonstrates characteristic anatomical findings. CCA step-offs and ECA flaps are relatively common and clinically insignificant, whereas ICA/CCA flaps and thrombi are less frequently seen and are associated with postoperative stroke/TIA.

Subependymal giant cell astrocytoma: diagnosis, screening, and treatment. Recommendations from the International Tuberous Sclerosis Complex Consensus Conference 2012.

BACKGROUND: Tuberous sclerosis complex is an autosomal dominant disorder predisposing to the development of benign lesions in different body organs, mainly in the brain, kidney, liver, skin, heart, and lung. Subependymal giant cell astrocytomas are characteristic brain tumors that occur in 10% to 20% of tuberous sclerosis complex patients and are almost exclusively related to tuberous sclerosis complex. Subependymal giant cell astrocytomas usually grow slowly, but their progression ultimately leads to the occlusion of the foramen of Monro, with subsequent increased intracranial pressure and hydrocephalus, thus necessitating intervention. During recent years, secondary to improved understanding in the biological and genetic basis of tuberous sclerosis complex, mammalian target of rapamycin inhibitors have been shown to be effective in the treatment of subependymal giant cell astrocytomas, becoming an alternative therapeutic option to surgery. METHODS: In June 2012, an International Tuberous Sclerosis Complex Consensus Conference was convened, during which an expert panel revised the diagnostic criteria and considered treatment options for subependymal giant cell astrocytomas. This article summarizes the subpanel's recommendations regarding subependymal giant cell astrocytomas. CONCLUSIONS: Mammalian target of rapamycin inhibitors have been shown to be an effective treatment of various aspects of tuberous sclerosis complex, including subependymal giant cell astrocytomas. Both mammalian target of rapamycin inhibitors and surgery have a role in the treatment of subependymal giant cell astrocytomas. Various subependymal giant cell astrocytoma-related conditions favor a certain treatment.

Correlation analysis of quantitative diffusion parameters in ipsilateral cerebral peduncle during Wallerian degeneration with motor function outcome after cerebral ischemic stroke.

BACKGROUND AND PURPOSE: To evaluate the time periods of Wallerian degeneration (WD) in which the diffusion parameters of ipsilateral corticalspinal tract (CST) can be used to predict the motor function outcome after brain infarction. METHODS: This retrospective study classified 48 diffusion tensor imaging patients with WD along CST into four groups based on the following time points after stroke onset, Group 1: within the first 2 weeks; Group 2: from 3 to 4 weeks; Group 3: from 5 to 14 weeks; Group 4: after 14 weeks. The apparent diffusion coefficient (ADC), fractional anisotropy (FA), and their ratios (=ipsilateral diffusion value/contralateral value) of cerebral peduncle were evaluated. The correlation between imaging parameters in each group and the motor function scores appraised at 8 months after stroke onset were assessed. RESULTS: There was no evident correlation of FA ratio (rFA) in Group 1 with motor function score (P = .05). The rFA and FA correlated with motor function score in other groups (P < .001 in each group). The ADC ratio and ipsilateral ADC value only showed significant correlation of with motor function score in Group 4 (P= .016 and .029, respectively). CONCLUSIONS: The rFA and ipsilateral FA values after 2 weeks of stroke onset correlate with the motor function outcome.

Coup de sabre presenting with worsening diplopia and enophthalmos.

A middle-aged woman with a diagnosis of linear scleroderma and systemic sclerosis presented with an atrophic skin lesion of the forehead extending in the right orbit and progressive diplopia in the right gaze. On exam, she had enophthalmos with a small, manifest esotropia in the right gaze. Orbital MRI revealed fat atrophy of the right upper eyelid and orbit not previously described. Inflammation and progressive collagen fibrosis involving subcutaneous tissue, fat, and muscle secondary to linear scleroderma may result in enophthalmos and diplopia.

Correlation of diffusion and perfusion MRI with Ki-67 in high-grade meningiomas.

OBJECTIVE: Atypical and anaplastic meningiomas have a greater likelihood of recurrence than benign meningiomas. The risk for recurrence is often estimated using the Ki-67 labeling index. The purpose of this study was to determine the correlation between Ki-67 and regional cerebral blood volume (rCBV) and between Ki-67 and apparent diffusion coefficient (ADC) in atypical and anaplastic meningiomas. MATERIALS AND METHODS: A retrospective review of the advanced imaging and immunohistochemical characteristics of atypical and anaplastic meningiomas was performed. The relative minimum ADC, relative maximum rCBV, and specimen Ki-67 index were measured. Pearson's correlation was used to compare these parameters. RESULTS: There were 23 cases with available ADC maps and 20 cases with available rCBV maps. The average Ki-67 among the cases with ADC maps and rCBV maps was 17.6% (range, 5-38%) and 16.7% (range, 3-38%), respectively. The mean minimum ADC ratio was 0.91 (SD, 0.26) and the mean maximum rCBV ratio was 22.5 (SD, 7.9). There was a significant positive correlation between maximum rCBV and Ki-67 (Pearson's correlation, 0.69; p = 0.00038). However, there was no significant correlation between minimum ADC and Ki-67 (Pearson's correlation, -0.051; p = 0.70). CONCLUSION: Maximum rCBV correlated significantly with Ki-67 in high-grade meningiomas.

Dual-energy CT angiography in the evaluation of intracranial aneurysms: image quality, radiation dose, and comparison with 3D rotational digital subtraction angiography.

OBJECTIVE: The purpose of this study was to evaluate the image quality, radiation dose, and diagnostic accuracy of dual-energy CT angiography (CTA) compared with 3D rotational digital subtraction angiography (DSA) in the detection of intracranial aneurysms. SUBJECTS AND METHODS: Forty-six patients with clinically suspected intracranial aneurysms underwent dual-source dual-energy CTA and 3D DSA. For the analysis of the image quality and radiation dose of dual-energy CTA, 46 patients who underwent digital subtraction CTA were recruited as a control group. The image quality of dual-energy CTA and digital subtraction CTA was rated on a 4-point scale as excellent, good, moderate, or poor. The radiation dose of CTA was recorded according to patient protocol. Aneurysm detection with dual-energy CTA compared with 3D DSA was analyzed on a per-patient and on a peraneurysm basis. Sensitivity, specificity, and positive and negative predictive values for aneurysm presence were determined. The mean maximum diameter and dome and neck dimensions of aneurysms were measured on dual-energy CTA and 3D DSA images. Correlation analysis between the two techniques was performed. RESULTS: There was no statistical difference between the image quality of dual-energy CTA and that of digital subtraction CTA (p>0.05). Patients undergoing dual-energy CTA received a smaller radiation dose (volume CT dose index, 20.6+/-0.1 mGy [mean+/-SD]; dose-length product, 398.6+/-19.0 mGy x cm) than those undergoing digital subtraction CTA (volume CT dose index, 50.4+/-3.4 mGy; dose-length product, 1,095.6+/-114.2 mGyxcm) (p<0.05). Three-dimensional DSA showed no aneurysm in 11 patients and 40 aneurysms in 35 patients. The mean maximum diameter of the aneurysms was 6+/-3 mm; the dome measurement, 5+/-3 mm; and the neck dimension, 3+/-2 mm. With dual-energy CTA, 38 aneurysms in 34 patients were correctly detected, and two aneurysms in two patients were missed. With DSA as the standard of reference, the sensitivity, specificity, and positive and negative predictive values of dual-energy CTA in the detection of intracranial aneurysm were 97.1%, 100%, 100%, and 91.7% on a per-patient basis and 95.0%, 100%, 100%, and 99.7% on a per-aneurysm basis. Dual-energy CTA had sensitivities of 93.8%, 100%, and 80.0% and specificities of 100%, 100%, and 100% in the detection of aneurysms larger than 5 mm, those measuring 3.1-5 mm, and aneurysms 3 mm or smaller. At dual-energy CTA, the mean maximum diameter and dome and neck dimensions were 6+/-3 mm, 5+/-3 mm, and 3+/-2 mm. Excellent correlation was found between DSA and dual-energy CTA findings with respect to mean maximum diameter and dome and neck dimensions (r=0.969, 0.957, and 0.870; p = 0.000). CONCLUSION: On the basis of the findings in the small series of patients evaluated, contrast-enhanced dual-energy CTA had diagnostic image quality at a lower radiation dose than digital subtraction CTA and high diagnostic accuracy compared with 3D DSA in the detection of intracranial aneurysms.

Conspicuity of diffuse axonal injury lesions on diffusion-weighted MR imaging.

OBJECTIVE: (1) To detect diffuse axonal injury (DAI) lesions by diffusion-weighted imaging (DWI), as compared with fluid-attenuated inversion recovery (FLAIR) imaging and (2) to evaluate hemorrhagic DAI lesions by b0 images obtained from DWI, as compared with gradient-echo (GRE) imaging. METHODS: We reviewed MR images of 36 patients with a diagnosis of DAI. MR imaging was performed 20 h to 14 days (mean, 3.7 days) after traumatic brain injury. We evaluated: (1) conspicuity of lesions on DWI and FLAIR and (2) conspicuity of hemorrhage in DAI lesions on b0 images and GRE imaging. RESULTS: DWI clearly depicted high-signal DAI lesions. The sensitivity of DWI to lesional conspicuity in DAI lesions was almost equal to that of FLAIR. The sensitivity of b0 images to identification of hemorrhagic DAI lesions was inferior to that of GRE. CONCLUSION: DWI is as useful as FLAIR in detecting DAI lesions. GRE imaging is still the superior tool for the evaluation of hemorrhagic DAI.